2006
DOI: 10.1016/j.lfs.2006.08.023
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The effects of G-CSF and naproxen sodium on the serum TGF-β1 level and fracture healing in rat tibias

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Cited by 16 publications
(12 citation statements)
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“…31 The rat as animal model for fracture studies. In general, the rat is predominantly used to study the effects of pharmaceuticals, [32][33][34][35][36][37][38][39][40] signalling proteins, and growth factors 38,41-44 on fracture healing with and without primary injury. Mechanical influences like ultrasound, 45 torsion stiffness 46 as well as compression and distraction 47 are examined as well but are not the predominant use for this fracture model.…”
Section: Animal Modelsmentioning
confidence: 99%
“…31 The rat as animal model for fracture studies. In general, the rat is predominantly used to study the effects of pharmaceuticals, [32][33][34][35][36][37][38][39][40] signalling proteins, and growth factors 38,41-44 on fracture healing with and without primary injury. Mechanical influences like ultrasound, 45 torsion stiffness 46 as well as compression and distraction 47 are examined as well but are not the predominant use for this fracture model.…”
Section: Animal Modelsmentioning
confidence: 99%
“…[40,41] There also is evidence that G-CSF treatment is associated with increased circulating TGF-β1 levels. [42] Together, these observations suggest the hypothesis that canonical TGF-β family signaling in bone marrow MSCs, by downregulating CXCL12 expression, may contribute to G-CSF induced HSC mobilization. To test this hypothesis, we first asked whether TGF-β1 regulates CXCL12 in primary murine bone marrow MSCs.…”
Section: Loss Of Smad4 In Mesenchymal Stromal Cells Does Not Affect Hmentioning
confidence: 85%
“…An earlier study reported that fracture healing in adult male rats could be accelerated by increased expression of TGF-β1 in both plasma and at the fracture site, when due to traumatic brain injury [ 29 ]. Another study revealed that the administration of naproxen sodium into bone fracture model rats decreased their TGF-β1 serum levels and resulted in a slow fracture healing for these rats, while the use of granulocyte colony stimulating factor (G-CSF) increased the TGF-β1 serum levels and led to a better fracture healing [ 30 ]. In addition, TGF-β1 released from TGF-β1-loaded microgranules promoted bone regeneration in rabbit calvarial defects after 4 weeks [ 31 ].…”
Section: Discussionmentioning
confidence: 99%